Most clinicians are aware of the pa

Most clinicians are aware of the pathological diagnosis of TCV PTC and its aggressive clinical behaviour, and the fact that some of these tumours arerefractory to radioactive iodine treatment.14,15 However, by examining the literature, one can easilydeduce that significant confusion exists among pathologists regarding the diagnosis of this tumour, whatpercentage of tumour needs to show diagnostic histology for it to be labelled as TCV PTC, and the specificmolecular features of this group that help in understanding its pathogenesis and also in predicting theprognosis.5,14,16 At present, there is not unanimousagreement on the percentage of TCV features requiredto diagnose an entire tumour as TCV PTC.16 To further add to this controversy, some authors in the pasthave designated TCV PTC as ‘poorly differentiated thyroid carcinoma’.17 It is not uncommon to find TCVpresenting as a minor component of the classic variant or other PTC with low-risk histology (usually 5–10%).5 It is important to mention the approximatepercentage of TCV PTC, as metastatic foci and locoregional recurrences of these cases may show higherpercentages or be entirely composed of TCV.Mutations of the BRAF proto-oncogene are morecommon in TCV PTC than in classic PTC.18 It hasbeen suggested that the aggressive behaviour of TCVPTC is due to these; BRAFV600E mutations in PTChave been associated with higher frequencies ofextraglandular extension and nodal metastases. Othernoted molecular findings in TCV PTC include loss ofheterozygosity for chromosome 1 (D1S243) and thep53 gene (TP53)19 and RET/PTC3 rearrangement.20The clinicopathological and molecular data available for TCV PTC highlight its aggressive clinicalbehaviour. Therefore, it is prudent for pathologists tocorrectly diagnose and report any foci of tall cellsregardless of their percentage. This will prompt theclinician to carefully monitor the patient after initialtreatment for recurrence, distant metastasis, andtransformation to anaplastic carcinoma.21